Premium
Activation of transcription factor Nrf2 to counteract mitochondrial dysfunction in Parkinson's disease
Author(s) -
BentoPereira Claudia,
DinkovaKostova Albena T.
Publication year - 2021
Publication title -
medicinal research reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.868
H-Index - 130
eISSN - 1098-1128
pISSN - 0198-6325
DOI - 10.1002/med.21714
Subject(s) - parkinson's disease , transcription factor , oxidative stress , disease , mitochondrion , neuroinflammation , biology , neuroscience , bioinformatics , medicine , genetics , gene , endocrinology
Parkinson's disease (PD) is a progressive neurodegenerative disorder, for which no disease‐modifying therapies are available to date. Although understanding of the precise aetiology of PD is incomplete, it is clear that age, genetic predisposition and environmental stressors increase the risk. At the cellular level, oxidative stress, chronic neuroinflammation, mitochondrial dysfunction and aberrant protein aggregation have been implicated as contributing factors. These detrimental processes are counteracted by elaborate networks of cellular defence mechanisms, one of which is orchestrated by transcription factor nuclear factor‐erythroid 2 p45‐related factor 2 (Nrf2; gene name NFE2L2 ). A wealth of preclinical evidence suggests that Nrf2 activation is beneficial in cellular and animal models of PD. In this review, we summarise the current understanding of mitochondrial dysfunction in PD, the role of Nrf2 in mitochondrial function and explore the potential of Nrf2 as a therapeutic target for mitochondrial dysfunction in PD.